Imbalance of Amniotic Fluid Activin-A and Follistatin in Intraamniotic Infection, Inflammation, and Preterm Birth

Hardy, John; Buhimschi, Irina A.; McCarthy, Megan; Zhao, Guomao; Laky, Christine; Shook, Lydia L.; Buhimschi, Catalin S.

doi:10.1210/jc.2015-4147

Cited by 15 publications

(18 citation statements)

References 43 publications

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“…ActRIIA is a transmembrane protein expressed on the surface of cell membranes. Activin signaling first activates ActRIIA, which phosphorylates type I receptors and then regulates the transcription of target genes through signal transduction via Smad classical or non-SMAD pathways [ 11 , 12 ]. The flow cytometry results showed that ActRIIA expression on CD8 + T cells and CD19 + B cells was increased in the Kawasaki disease group compared with the healthy control group.…”

Section: Resultsmentioning

confidence: 99%

Activin a suppresses peripheral CD8+ T lymphocyte activity in acute-phase Kawasaki disease

Weng

et al. 2021

BMC Immunol

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Background Kawasaki disease is an autoimmune disease characterized by systemic vasculitis of unknown aetiology and most commonly occurs in children under 5 years old. Previous studies have found that the over-activation of lymphocytes is an important mechanism of Kawasaki disease. Activin A, also known as immunosuppressive factor P, is a multifunctional growth and transforming factor. However, whether activin A is involved in the regulation of peripheral lymphocytes activity in Kawasaki disease is unclear. Thus, we aimed to investigate the effect of activin A on the activity of peripheral lymphocytes in acute-phase Kawasaki disease. Methods Seven patients with Kawasaki disease and seven healthy controls were studied. Peripheral blood lymphocytes were isolated by Ficoll density gradient centrifugation. The activation of CD4+ and CD8+ T cells and CD19+ B cells was investigated by flow cytometry. The expression of activin type IIA receptors was investigated by flow cytometry. Results Immune imbalance in CD4 and CD8 lymphocytes were detected in acute-phase Kawasaki disease. The expression of activin type IIA receptors on CD8+ T cells and CD19+ B cells was increased in acute-phase Kawasaki disease and decreased following treatment with activin A. Activin A suppressed the expression of CD25 and CD69 on CD8+ T cells and the expression of CD69 on CD19+ B cells. Conclusions The expression of activin type IIA receptor was increased on CD8+ T cells and CD19+ B cells in Kawasaki disease. Activin A suppressed the expression of CD25, CD69 and activin type IIA receptors on peripheral CD8+ T lymphocyte. Activin A plays different roles in different lymphocyte subsets and suppresses peripheral CD8+ T lymphocyte activity in acute-phase Kawasaki disease.

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Section: Resultsmentioning

confidence: 99%

Activin a suppresses peripheral CD8+ T lymphocyte activity in acute-phase Kawasaki disease

Weng

et al. 2021

BMC Immunol

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“…An increasing number of clinical studies have reported that activin A levels are markedly elevated during the various bacterial infections, including sepsis, meningitis and intra-amniotic infection, and so on ( Ebert et al., 2006 ; Hardy et al., 2016 ; Lee et al., 2016 ; Michel et al., 2003 ; Petrakou et al., 2013 ; Rosenberg et al., 2012 ; Wilms et al., 2010 ). Higher levels of serum activin A have been observed in patients with sepsis compared to healthy volunteers, and activin A levels were correlated with disease severity in these patients, suggesting that activin A may serve as a potential diagnostic marker for sepsis severity ( Lee et al., 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Activin A impairs ActRIIA+ neutrophil recruitment into infected skin of mice

Jiang

et al. 2021

iScience

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Summary Activin A levels are elevated during multiple severe infections and associated with an increased risk of death. However, the role of activin A in bacterial infection is still unclear. Here, we found that activin A levels were increased during S. aureus skin infection in mice. Administration of activin A increased the bacterial burden and promoted the spread of bacteria in vivo . Moreover, activin A inhibited neutrophil chemotaxis to N-formylmethionine-leucyl-phenylalanine via the type IIA activin receptor (ActRIIA) in vitro and impaired ActRIIA + neutrophil recruitment to infection foci in vivo . Additionally, we identified a novel subpopulation of neutrophils, ActRIIA + neutrophils, which exhibit superior phagocytic capacity compared to ActRIIA − neutrophils and possess an N2-like immunoregulatory activity via secreting IL-10 and TGF-β. Taken together, these findings indicate that activin A inhibits the recruitment of ActRIIA + neutrophils to infected foci, leading to the impairment of bacterial clearance, and thus may hamper early infection control.

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“…In contrast to activin, FS has an anti-inflammatory response by direct inhibition of activin (29). The imbalance between activin and FS exaggerates the severity of the inflammatory state in diseases such as asthma and carcinogenesis (30). The release of activin precedes the release of other inflammatory cytokines, therefore the modulation of the activin and FS system is a potential therapeutic target in HIVassociated PE which has an inflammatory component (30).…”

Section: Discussionmentioning

confidence: 99%

“…The imbalance between activin and FS exaggerates the severity of the inflammatory state in diseases such as asthma and carcinogenesis (30). The release of activin precedes the release of other inflammatory cytokines, therefore the modulation of the activin and FS system is a potential therapeutic target in HIVassociated PE which has an inflammatory component (30). The non-significant difference in FS expression in this study may be attributed to the use of highly active antiretroviral therapy (HAART), a standard of care in all HIV infected patients in SA.…”

Section: Discussionmentioning

confidence: 99%

The role of follistatin and granulocyte-colony stimulating factor in HIV-associated pre-eclampsia

Mdlalose

Moodley

Naicker

2020

Pregnancy Hypertension

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I, Siphesihle Mdlalose declare that: i.The research reported in this dissertation, except where otherwise indicated is my original work.ii. This dissertation has not been submitted for any degree or examination at any other university.iii. This dissertation does not contain other person's data, pictures, graphs or other information, unless specifically acknowledged as being sourced from other persons. iv. This dissertation does not contain other persons writing, unless specifically acknowledged as being sourced from other researchers. Where other sources have been quoted, then: a. Their words have been rewritten but the general information attributed by them has been referenced. b. Where their exact words have been used their writing has been placed inside quotation marks and referenced. v. Where I have reproduced a publication of which I am the author, co-author, I have indicated in detail which part of the publication was actually written by myself alone and have fully referenced such publications.vi. This dissertation does not contain text, graphics, or tables copied and pasted from the internet, unless specifically acknowledged and the source being detailed in the dissertation and the reference sections.

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Imbalance of Amniotic Fluid Activin-A and Follistatin in Intraamniotic Infection, Inflammation, and Preterm Birth

Abstract: Activin-A and follistatin are part of the complex inflammatory response of the gestational sac to infection and modulate effector pathways leading to PTB. The activin-A to follistatin ratio may play a role in determining the clinical phenotype of PTB as preterm labor or PPROM.

Cited by 15 publications

References 43 publications

Activin a suppresses peripheral CD8+ T lymphocyte activity in acute-phase Kawasaki disease

Activin a suppresses peripheral CD8+ T lymphocyte activity in acute-phase Kawasaki disease

Activin A impairs ActRIIA+ neutrophil recruitment into infected skin of mice

The role of follistatin and granulocyte-colony stimulating factor in HIV-associated pre-eclampsia

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